Evidence map›Paper›PMID 23791709›Full record

ReviewNeurochemistry international2013

Regulation of astrocyte glutamine synthetase in epilepsy.

Tore Eid, Nathan Tu, Tih-Shih W Lee, James C K Lai

Abstract readReview
In one paragraph

Review in Neurochemistry international, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed, 1 pooled it
4.5field-weighted citation impact, top 4% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

61 citing papers in PubMed, 1 synthesis or guideline pooled it, 108 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Article
  5. TREK-1 and epilepsy: regulating the balance of KBehavioral and brain functions : BBF · 2025
    Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Neuroglia and brain energy metabolism.Handbook of clinical neurology · 2025
    Review
  11. Review
  12. Article
  13. Article
  14. Review
  15. Review
  16. Review
  17. Article
  18. Review
  19. Review
  20. Astrocytes: GABAceptive and GABAergic Cells in the Brain.Frontiers in cellular neuroscience · 2022
    Review

1 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 2 institutions in 1 country.

Tore EidDepartment of Laboratory Medicine, Yale University School of Medicine, New Haven, CT 06520, United States. Electronic address: tore.eid@yale.edu.
Nathan Tu
Tih-Shih W Lee
James C K Lai
Yale University · USIdaho State University · US

Funding

YALE UNIVERSITY CLINICAL AND TRANSLATIONAL SCIENCE AWARD PROGRAMUL1RR024139 · NCRR · YALE UNIVERSITY · PI SHERWIN, ROBERT S · 2006 to 2011
$56.8M
Yale University Clinical and Translational Science Award ProgramTL1RR024137 · NCRR · YALE UNIVERSITY · PI SHERWIN, ROBERT S · 2006 to 2011
$3.2M
Glutamine Synthetase and the Mechanism of Seizures in Mesial Temporal Lobe EpilepR01NS070824 · NINDS · YALE UNIVERSITY · PI EID, TORE · 2010 to 2014
$1.9M
Dysregulation of Glutamine Synthetase in Human Temporal Lobe EpilepsyK08NS058674 · NINDS · YALE UNIVERSITY · PI EID, TORE · 2008 to 2012
$867k
NCRR NIH HHS TL1 RR024137NCRR NIH HHS UL1 RR024139NINDS NIH HHS K08 NS058674NINDS NIH HHS R01 NS070824
6 · The paper itself

Abstract

Astrocytes play a crucial role in regulating and maintaining the extracellular chemical milieu of the central nervous system under physiological conditions. Moreover, proliferation of phenotypically altered astrocytes (a.k.a. reactive astrogliosis) has been associated with many neurologic and psychiatric disorders, including mesial temporal lobe epilepsy (MTLE). Glutamine synthetase (GS), which is found in astrocytes, is the only enzyme known to date that is capable of converting glutamate and ammonia to glutamine in the mammalian brain. This reaction is important, because a continuous supply of glutamine is necessary for the synthesis of glutamate and GABA in neurons. The known stoichiometry of glutamate transport across the astrocyte plasma membrane also suggests that rapid metabolism of intracellular glutamate via GS is a prerequisite for efficient glutamate clearance from the extracellular space. Several studies have indicated that the activity of GS in astrocytes is diminished in several brain disorders, including MTLE. It has been hypothesized that the loss of GS activity in MTLE leads to increased extracellular glutamate concentrations and epileptic seizures. Understanding the mechanisms by which GS is regulated may lead to novel therapeutic approaches to MTLE, which is frequently refractory to antiepileptic drugs. This review discusses several known mechanisms by which GS expression and function are influenced, from transcriptional control to enzyme modification.

Indexed as

AstrocytesEpilepsy, Temporal LobeGlutamate-Ammonia LigaseHumansGlutamate-Ammonia LigaseGliosisGlutamateHippocampal sclerosisLimbic systemMetabolismSeizures

Identifiers

PMID23791709
PMCPMC3825815
OpenAlexW2002196897

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.